Báo cáo y học: "RANKL increases the level of Mcl-1 in osteoclasts and reduces bisphosphonate-induced osteoclast apoptosis in vitro"

Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học General Psychiatry cung cấp cho các bạn kiến thức về ngành y đề tài: RANKL increases the level of Mcl-1 in osteoclasts and reduces bisphosphonate-induced osteoclast apoptosis in vitro. | Available online http content 11 2 R58 Research article RANKL increases the level of Mcl-1 in osteoclasts and reduces bisphosphonate-induced osteoclast apoptosis in vitro Karen A Sutherland Helena L Rogers Denise Tosh and Michael J Rogers Bone Musculoskeletal Research Programme School of Medicine Dentistry Institute of Medical Sciences University of Aberdeen Foresterhill Aberdeen AB25 2ZD UK Contributed equally Corresponding author Michael J Rogers Received 25 Jun 2008 Revisions requested 31 Jul 2008 Revisions received 8 Apr 2009 Accepted 30 Apr 2009 Published 30 Apr 2009 Arthritis Research Therapy 2009 11 R58 doi ar2681 This article is online at http content 11 2 R58 2009 Sutherland et al. licensee BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License http licenses by which permits unrestricted use distribution and reproduction in any medium provided the original work is properly cited. Open Access Abstract Introduction Bisphosphonates are the most widely used class of drug for inhibiting osteoclast-mediated bone loss but their effectiveness at preventing joint destruction in rheumatoid arthritis has generally been disappointing. We examined whether the ability of bisphosphonates to induce osteoclast apoptosis and inhibit bone resorption in vitro is influenced by the cytokine receptor activator of nuclear factor-kappa B ligand RANKL an important mediator of inflammation-induced bone loss. Methods Rabbit osteoclasts were treated with the bisphosphonates clodronate or alendronate for up to 48 hours in the absence or presence of RANKL. Changes in cell morphology and induction of apoptosis were examined by scanning electron microscopy whilst resorptive activity was determined by measuring the area of resorption cavities. Changes in the level of anti-apoptotic proteins including Mcl-1 Bcl-2 and Bcl-x L

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